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Journal of Bacteriology, January 2006, p. 141-149, Vol. 188, No. 1
0021-9193/06/$08.00+0     doi:10.1128/JB.188.1.141-149.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Role of Salmonella enterica Serovar Typhimurium Two-Component System PreA/PreB in Modulating PmrA-Regulated Gene Transcription

Massimo Merighi,1,{dagger},§ Amanda Carroll-Portillo,2,{ddagger},§ Alecia N. Septer,1 Aditi Bhatiya,1 and John S. Gunn1*

Department of Molecular Virology, Immunology, and Medical Genetics and Center for Microbial Interface Biology, The Ohio State University, 333 W. 10th Avenue, Columbus, Ohio 43210,1 University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, Texas 782292

Received 25 August 2005/ Accepted 6 October 2005

The PmrA/PmrB two-component system encoded by the pmrCAB operon regulates the modification of Salmonella enterica serovar Typhimurium lipopolysaccharide leading to polymyxin B resistance. PmrA and PhoP are the only known activators of pmrCAB. A transposon mutagenesis screen for additional regulators of a pmrC::MudJ fusion led to the identification of a two-component system, termed PreA/PreB (pmrCAB regulators A and B), that controls the transcription of the pmrCAB operon in response to unknown signals. The initial observations indicated that insertions in, or a deletion of, the preB sensor, but not the preA response regulator, caused upregulation of pmrCAB. Interestingly, the expression of pmrCAB was not upregulated in a preAB mutant grown in LB broth, implicating PreA in the increased expression of pmrCAB in the preB strain. This was confirmed by overexpression of preA+ in preAB or preB backgrounds, which resulted in significant upregulation or further upregulation of pmrCAB. No such effect was observed in any tested preB+ backgrounds. Additionally, an ectopic construct expressing a preA[D51A] allele also failed to upregulate pmrC in any of the pre backgrounds tested, which implies that there is a need for phosphorylation in the activation of the target genes. The observed upregulation of pmrCAB occurred independently of the response regulators PmrA and PhoP. Although a preB mutation led to increased transcription of pmrCAB, this did not result in a measurable effect on polymyxin B resistance. Our genetic data support a model of regulation whereby, in response to unknown signals, the PreB sensor activates PreA, which in turn indirectly upregulates pmrCAB transcription.

* Corresponding author. Mailing address: Department of Molecular Virology, Immunology, and Medical Genetics and Center for Microbial Interface Biology, The Ohio State University, 270 TMRF, 420 W. 12th Avenue, Columbus, OH 43210. Phone: (614) 292-6036. Fax: (614) 292-5495. E-mail: gunn.43{at}osu.edu.

{dagger} Present address: Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115.

§ M.M. and A.C.-P. contributed equally to this work.

{ddagger} Present address: Department of Biomolecular Materials and Interfaces, Sandia National Laboratories, Albuquerque, NM 87185.

Journal of Bacteriology, January 2006, p. 141-149, Vol. 188, No. 1
0021-9193/06/$08.00+0     doi:10.1128/JB.188.1.141-149.2006
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



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